Outbreaks of stringhalt in northern California.
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Animals↗
Biomedical subjects
F D Galey
Publications and source records attributed to F D Galey.
Field investigations of small animal toxicoses.
An in-depth investigation of a small animal poisoning case resembles a thorough version of the traditional farm call that is provided by large animal clinicians. Goals of such investigations are to diagnose cases, identify responsible toxicants and their sources, and to make recommendations regarding treatment and prevention of further occurrences. The detailed history, interviews, site visit, record keeping, and analysis of findings are discussed.
Animals↗
Lead concentrations in blood and milk from periparturient dairy heifers seven months after an episode of acute lead toxicosis.
In September 1988, 100 of 300 yearling dairy heifers developed blindness, tachypnea, foaming at the mouth, chewing, and facial fasciculations. Twenty-five animals died. Lead toxicosis was diagnosed based on the clinical signs and the presence of excessive concentrations of lead in whole blood, liver, kidney, and rumen contents of affected animals. The source of the lead was sudan grass silage that had been contaminated by soil that contained up to 77,000 mg/kg of lead. Lead concentrations were determined approximately 7 months after the acute episode of lead toxicosis. Whole blood and milk samples were obtained from heifers and a group of control cows 2 weeks prior to (blood only), at the time of, and 2 and 4 weeks after freshening. No lead was found in any of the milk samples (detection limit = 0.055 mg/liter). Animals that had been severely affected by lead toxicosis experienced a transient increase in whole blood lead concentrations at freshening that was not high enough to be considered toxic. No similar increases in blood lead were observed for control cows or heifers that had experienced milder toxicosis. These findings suggest that at parturition lead is mobilized into the blood of cattle previously exposed to excessive lead.
Animals↗
A case of Datisca glomerata poisoning in beef cattle.
Six of 175 Angus heifers died after ingesting excessive amounts of Durango root (Datisca glomerata). Animals had rumens full of Durango root, were extremely lethargic, and had diarrhea prior to death. The animals had nonspecific postmortem lesions. This case is discussed in light of previous findings from trials in which Durango root was experimentally fed to cattle.
Animals↗
Effect of an aqueous extract of black walnut (Juglans nigra) on isolated equine digital vessels.
An aqueous extract was made from black walnut (Juglans nigra) heartwood obtained in the fall of the year. Ten hours after nasogastric administration of 5 L of the extract, a 550-kg, 13-yr-old Quarter Horse gelding experienced Obel grade-3 laminitis. The effect of aqueous extract of black walnut on vascular contractility was then tested, using isolated equine digital arteries and veins. The vessels were maintained in Krebs bicarbonate buffer with 95% oxygen at 37 C. The extract did not induce a direct contractile effect. It did, however, reversibly enhance the vasoconstriction induced in the isolated vessels by administration of epinephrine potentiated with hydrocortisone. In contrast, aqueous extracts made, using the same techniques, from the shavings of eastern white pine (Pinus strobus), eastern red cedar (Juniperus virginiana), and pin oak (Quercus palustrus) had no effect on epinephrine-induced digital vessel contractions.
Animals↗
Gamma scintigraphic analysis of the distribution of perfusion of blood in the equine foot during black walnut (Juglans nigra)-induced laminitis.
Twelve horses, with acute laminitis (primarily in the forefeet) at 12 hours after intragastric dosing with an aqueous extract of black walnut (Juglans nigra) heart-wood, were studied. The distribution of perfusion of blood to the foot and to outlined regions within the foot was quantified, using gamma scintigraphy of regionally infused 99mTc-labeled macroaggregated albumin, before and 12 hours after extract administration. Horses 1 to 3 were not studied further. Perfusion was quantified again for horses 4 to 12 at 84 hours after extract administration. At the onset of acute laminitis, horses 7 to 12 were administered a single dose of prazosin (0.025 mg/kg of body weight, IV) immediately after scintigraphy of the right forelimb and before scintigraphy of the left forelimb. When compared with baseline images, perfusion to the forefoot of horses after the development of acute laminitis was quantitatively decreased vs perfusion to the entire distal portion of the forelimb. Also with the onset of laminitis, perfusion also decreased to the dorsal laminar and coronary corium regions vs the distal portion of the forelimb. The acute laminitis-associated deficit in perfusion to the dorsal laminitis-associated deficit in perfusion deficit in perfusion to either the coronary corium or the entire forefoot. Equivalent deficits in the distribution of perfusion were not detected in forelimbs from horses with acute laminitis and which had been treated with prazosin. When compared with baseline images, perfusion to the dorsal lamina was increased in relation to perfusion to the distal portion of the limb at postdosing hour 84. Prazosin treatment did not influence that increase in perfusion to the dorsal lamina.
Animals↗
A case of scleroderma citrinum poisoning in a miniature Chinese pot-pellied pig.
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Animals↗
Antagonism in isolated equine digital vessels of contraction induced by epinephrine in the presence of hydrocortisone and an aqueous extract of black walnut (Juglans nigra).
Prazosin, isoxsuprine, and nifedipine were screened for ability to reverse contraction of isolated equine digital vascular strips produced by epinephrine (Epi) in the presence of hydrocortisone (Hc) and an aqueous extract of black walnut (Juglans nigra) (BW). Two arteries and two veins from each of three horses for each drug (n = 9) were maintained in isolated tissue baths in Krebs' bicarbonate buffer with 95% oxygen at 37 degrees C. Six-point Epi concentration-response (C-R) curves were obtained for each vessel in the presence of Hc, BW, and the appropriate vehicle. This was repeated for each vessel using one of two concentrations of one of the three test drugs. Each drug and concentration combination was tested on a total of three arteries and three veins. Prazosin produced a concentration-dependent shift of the Epi C-R curve to the right but the curve maintained the same maximum height and slope, which is consistent with competitive alpha 1 adrenergic blockade. Isoxsuprine exhibited similar behavior, although the precise mechanism of action for isoxsuprine is unknown. Conversely, nifedipine did not shift the curve but did depress maximum contraction, suggesting a non-competitive interaction consistent with its mechanism of calcium-channel blockade.
Animals↗
Therapeutic efficacy of superactive charcoal in rats exposed to oral lethal doses of T-2 toxin.
Superactive charcoal, a compound known to complex with many toxins, was evaluated in this study for its effectiveness in preventing death in rats given an oral lethal dose of 8 mg/kg body weight of T-2 toxin. The median effective dose of oral superactive charcoal in preventing deaths in rats was 0.175 g/kg body weight. Concurrent use of cathartics, such as sorbitol, magnesium sulfate and sodium sulfate, to facilitate removal of the superactive charcoal:T-2 toxin complex formed in vivo did not enhance the survival rates of rats. One gram per kilogram body weight oral superactive charcoal enhanced survival times and survival rates in rats given 8 mg/kg of T-2 toxin as late as 3 hr after the T-2 toxin was administered. Some benefit in survival rate may be derived from giving the superactive charcoal as late as 5 hr after the T-2 toxin.
Administration, Oral↗
Blue-green algae (Microcystis aeruginosa) hepatotoxicosis in dairy cows.
Twenty cows from a dairy herd consisting of 60 healthy, lactating Holsteins developed clinical signs of anorexia, mental derangement, dehydration, recumbency, and ruminal atony after ingesting water containing blue-green algae. Of the 20 cows, 9 died. The algal bloom, which developed in a stagnant pond during hot, dry weather, was identified as the cyanobacterium Microcystis aeruginosa, a potentially hepatotoxic algae. One week after the onset of toxicosis, affected cows seemed healthy, although liver-associated enzyme activities (alkaline phosphatase, gamma-glutamyl transferase, aspartate transaminase, and lactate dehydrogenase) were increased. Intraruminal administration of the intact wet bloom to a healthy 125-kg Angus heifer was followed by hepatic necrosis and death. The liver was large, friable, and gun-metal blue, with microscopically evident hepatocyte dissociation, degeneration, and necrosis. The ingesta of the heifer contained typical clumps of cells that were identified as M aeruginosa. The intraperitoneal administration of lyophilized cell material from that bloom to 18 mice caused marked hepatic enlargement. The intraperitoneal median lethal dose of the dried bloom was estimated to be 10 mg/kg of body weight. A cyclic peptide toxin purified from the algae seems to be similar structurally to toxins from other characterized hepatotoxic blooms of M aeruginosa.
Animals↗
Intramuscular selenium administration in selenium-deficient cattle.
Nine recently weaned Hereford heifers were randomly assigned to a control group (n = 3) or a treatment group (n = 6). The animals were selenium (Se) deficient (mean +/- SD blood Se concentration = 0.024 +/- 0.012 microgram/mL). They were maintained on a selenium-deficient diet, and on day 0 of the study the treatment group was given 0.05 mg Se/kg body weight intramuscularly, while the control group received a placebo. The Se concentration of blood, serum, and urine as well as the glutathione peroxidase (GSH-Px) activity of blood and serum was measured over an 84-day period. Peak blood Se and serum Se concentrations (mean +/- SD) in the treatment group occurred at 5 hours postinjection and were 0.131 +/- 0.028 microgram/mL and 0.154 +/- 0.027 microgram/mL, respectively. The mean blood Se concentration of the treatment group was greater (P < .05) than that of the control group for the first 28 days after injection. The mean serum Se concentration of the treatment group was greater (P < .05) than that of the control group for all times after injection, except for day 56. The mean (+/- SD) blood GSH-Px activity of the treatment group (12.0 +/- 2.3 mU/min/mg hemoglobin) was increased (P < .05) over the control group (2.0 +/- 1.4 mU/min/mg hemoglobin) by day 28 and continued to be greater (P < .05) throughout the 84 day postinjection period.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Neurotoxic mycotoxins: a review of fungal toxins that cause neurological disease in large animals.
Five mycotoxins found in concentrates or roughages have been shown to cause neurologic disease in livestock. Fumonisin B1 is produced by Fusarium moniliforme and causes leukoencephalomalacia in horses. Swainsonine and slaframine are produced by Rhizoctonia leguminicola and cause mannose accumulation and parasympathomimetic effects, respectively. Lolitrems from Acremonium lolii and paspalitrems from Claviceps paspali are tremorgens found in grasses.
Alkaloids↗
Recurrent transient paresis in a turkey flock.
Recurring episodes of extreme leg weakness and associated mortality were documented in a turkey flock at 8 to 15 weeks of age. Flock mortality attributed to posterior paresis was approximately 12%, or 4800 of 40,000 turkeys. Four of six open-confinement units were affected. Gross and histological examinations revealed no significant lesions. Immunology and virology were uninformative. There were no significant differences in serum chemistry between clinically affected and normal turkeys. Testing of feed, water, soil, and tissues revealed no common toxicants. Isolation and supportive care for affected turkeys, both in the laboratory and in the field, frequently resulted in full recovery. Injection of a test group of affected turkeys with Type C botulism antitoxin appeared to enhance recovery. However, repeated attempts to detect botulism toxin in serum, liver, or cecal contents using mouse bioassay procedures were unsuccessful.
Animals↗
A syndrome in commercial turkeys in California and Oregon characterized by a rear-limb necrotizing skeletal myopathy.
A necrotizing skeletal myopathy of rear limbs was diagnosed in 17 flocks of commercial turkeys. The mean mortality attributed to the myopathy was 2.29% (range = 0.13-9.7%) over a mean period of 9.6 days (range = 6-14 days). The mean age of the birds at the time of onset was 7.4 weeks (range = 4-10.5 weeks). Clinically, birds experienced an episode of watery droppings and high-pitched crying, followed by rear-limb paresis or paralysis. Creatine kinase and aspartate aminotransferase were markedly elevated in birds with the myopathy. Grossly, a few birds had pale streaking in the muscles of the thighs and legs. Histologically, acute and subacute degeneration was present in myofibers of the legs, abdomen, thighs, back, and tail. The subacute lesion was characterized by marked sarcolemmal cell proliferation. Feed analyses ruled out selenium deficiency and the presence of mycotoxins as etiologies. Monensin was present in approved usage or only slightly elevated levels. A known potentiating antibiotic was being used concurrently with monensin in only one flock.
Animals↗
Zinc toxicosis due to ingestion of a penny in a gray-headed chachalaca (Ortalis cinereiceps).
Zinc toxicosis was diagnosed in a gray-headed chachalaca (Ortalis cinereiceps) due to ingestion of a copper-plated zinc penny. Histopathological lesions were most marked in the pancreas. These lesions included apoptosis, zymogen granule depletion, and loss of normal acinar architecture. There was also severe gizzard erosion. Heavy metal analysis revealed abnormal levels of zinc and iron in the liver. Iron pigment in the liver was most concentrated in Kupffer cells. This, along with evidence of erythrophagocytosis in the spleen, suggested that extravascular hemolysis was also associated with zinc toxicosis in this case.
Animals↗
A rapid multiresidue screen for organophosphorus, organochlorine, and N-methyl carbamate insecticides in plant and animal tissues.
A multiresidue screen for the quantitative determination of 43 organophosphorus, 17 organochlorine, and 11 N-methyl carbamate insecticides in 10 g of plant or animal tissues is described. The insecticides are extracted with 5% ethanol in ethyl acetate (v/v). Samples with high lipid content are cleaned up by automated gel permeation chromatography with a 30% ethyl acetate in hexane (v/v) eluant and in-line silica gel minicolumns. Highly pigmented samples are cleaned up with class-specific solid-phase extraction columns. The concentrated extracts are analyzed by selective detection with gas chromatography or liquid chromatography. Recovery of 71 insecticides ranged from 77 to 113%. Analysis of fortified bovine liver (n = 5) resulted in an average recovery of 96 +/- 4% at the 0.5 to 0.05 micrograms/g level. Analysis of fortified alfalfa hay (n = 5) resulted in a mean recovery of 94 +/- 4% at the 0.06 to 0.5 micrograms/g level, and analysis of fortified fresh tomatoes (n = 5) resulted in an average recovery of 97 +/- 3% at the 0.06 to 0.5 micrograms/g level. Method detection limits ranged from 0.02 to 0.5 micrograms/g for the compounds studied with a nominal 10 g sample.
Acetates↗
Determination of cholinesterase activity in brain and blood samples using a plate reader.
A rapid method is described for the quantitative determination of cholinesterase activity in large batches of blood and brain samples. The technique is an adaptation of the Ellman procedure for a 96-well microtiter plate reader. Ten samples can be analyzed simultaneously in 5 min, with all calculations, including statistical analysis, done automatically. The method detection limit is 0.1 microM/mL/min for blood and 0.1 microM/g/min for brain samples. The procedure has been applied to the routine analyses of samples presented to the veterinary diagnostic laboratory. Method performance, quality control, and normal ranges of cholinesterase activity in livestock and other animals are described.
Animals↗
Skeletal myopathy produced with experimental dosing of turkeys with monensin.
Monensin was given via gavage to 5- and 6-week-old broad-breasted white turkeys. The birds were allotted into four groups--three groups given monensin and one group of controls--in two experimental trials. Treated turkeys in Trial 1 received one dose of monensin per day for 4 days at 4.7 mg monensin/kg body weight, 8.8 mg/kg, or 17.6 mg/kg. Treated turkeys in Trial 2 received one dose of monensin per day for 5 days at 1.93 mg/kg, 4.7 mg/kg, or 8.8 mg/kg. Turkeys receiving the lowest dose showed no clinical signs of myopathy. Birds receiving 4.7 mg monensin/kg developed ataxia after the third dose and rear limb paresis and paralysis after the fifth dose. Turkeys receiving 8.8 mg/kg were ataxic after the second dose and paretic or paralyzed after the fourth dose. Turkeys receiving 17.6 mg/kg were ataxic 3 hours after the first dose and paretic or paralyzed 8 hours after the first dose. Histologically, a necrotizing skeletal myopathy was present in the muscles of the rear limbs. A dose-related response was observed in the percentage of myofibers damaged in birds that survived until the end of the trials. Intrafiber edema and vacuolation were observed in histologic sections from myocardium of turkeys from the two highest dose groups.
Animals↗